title: Redox-modulated phenomena and radiation therapy: the central role of superoxide dismutases.
abstract: CONCLUSIONS
  Ionizing radiation is a vital component in the oncologist's arsenal for the treatment of cancer. Approximately 50% of all cancer patients will receive some form of radiation therapy as part of their treatment regimen. DNA is considered the major cellular target of ionizing radiation and can be damaged directly by radiation or indirectly through reactive oxygen species (ROS) formed from the radiolysis of water, enzyme-mediated ROS production, and ROS resulting from altered aerobic metabolism.
  
  
  BACKGROUND
  ROS are produced as a byproduct of oxygen metabolism, and superoxide dismutases (SODs) are the chief scavengers. ROS contribute to the radioresponsiveness of normal and tumor tissues, and SODs modulate the radioresponsiveness of tissues, thus affecting the efficacy of radiotherapy.
  
  
  RESULTS
  Despite its prevalent use, radiation therapy suffers from certain limitations that diminish its effectiveness, including tumor hypoxia and normal tissue damage. Oxygen is important for the stabilization of radiation-induced DNA damage, and tumor hypoxia dramatically decreases radiation efficacy. Therefore, auxiliary therapies are needed to increase the effectiveness of radiation therapy against tumor tissues while minimizing normal tissue injury.
  
  
  CONCLUSIONS
  Because of the importance of ROS in the response of normal and cancer tissues to ionizing radiation, methods that differentially modulate the ROS scavenging ability of cells may prove to be an important method to increase the radiation response in cancer tissues and simultaneously mitigate the damaging effects of ionizing radiation on normal tissues. Altering the expression or activity of SODs may prove valuable in maximizing the overall effectiveness of ionizing radiation.
authors.affiliation: 1 Graduate Center for Toxicology, University of Kentucky , Lexington, Kentucky.
authors.forename: Aaron K
authors.initials: AK
authors.lastname: Holley
authors.forename: Lu
authors.initials: L
authors.lastname: Miao
authors.forename: Daret K
authors.initials: DK
authors.lastname: St Clair
authors.forename: William H
authors.initials: WH
authors.lastname: St Clair
mesh_terms: D000818:Animals; D024201:Bystander Effect / Q000528:radiation effects; D015687:Cell Hypoxia / Q000528:radiation effects; D004249:DNA Damage; D006801:Humans; D009369:Neoplasms / Q000201:enzymology / Q000473:pathology / Q000532:radiotherapy*; D010084:Oxidation-Reduction; D011836:Radiation Tolerance; D013482:Superoxide Dismutase / Q000502:physiology*
chemical_list: D013482:Superoxide Dismutase